Wnt Signaling: Paths for Cancer Progression

Carreira-Barbosa, Filipa; Nunes, Sónia

doi:10.1007/978-3-030-34025-4_10

Cited by 16 publications

(14 citation statements)

References 109 publications

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“…Scheller et al demonstrated that the canonical Wnt/β-catenin signaling pathway inhibits the expression of odontoblast-specific genes during odontogenic differentiation of hDPSCs [ [24] , [42] ]. Moreover, Wnt10a, a Wnt agonist, was reported to negatively regulate odontoblastic differentiation of hDPSCs [ 15 , [25] , [43] ]. Conversely, other studies have shown that the Wnt/β-catenin signaling pathway can promote the odontogenic differentiation of the hDPSCs.…”

Section: Discussionmentioning

confidence: 99%

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Treated dentin matrix induces odontogenic differentiation of dental pulp stem cells via regulation of Wnt/β-catenin signaling

Liu

Sun

Yuan

et al. 2022

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Treated dentin matrix (TDM) is an ideal scaffold material containing multiple extracellular matrix factors. The canonical Wnt signaling pathway is necessary for tooth regeneration. Thus, this study investigated whether the TDM can promote the odontogenic differentiation of human dental pulp stem cells (hDPSCs) and determined the potential role of Wnt/β-catenin signaling in this process. Different concentrations of TDM promoted the dental differentiation of the hDPSCs and meanwhile, the expression of GSK3β was decreased. Of note, the expression of the Wnt/β-catenin pathway-related genes changed significantly in the context of TDM induction, as per RNA sequencing (RNA seq) data. In addition, the experiment showed that new dentin was visible in rat mandible cultured with TDM, and the thickness was significantly thicker than that of the control group. In addition, immunohistochemical staining showed lower GSK3β expression in new dentin. Consistently, the GSK3β knockdown hDPSCs performed enhanced odotogenesis compared with the control groups. However, GSK3β overexpressing could decrease odotogenesis of TDM-induced hDPSCs. These results were confirmed in immunodeficient mice and Wistar rats. These suggest that TDM promotes odontogenic differentiation of hDPSCs by directly targeting GSK3β and activating the canonical Wnt/β-catenin signaling pathway and provide a theoretical basis for tooth regeneration engineering.

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Section: Discussionmentioning

confidence: 99%

“…It continuously phosphorylates β-catenin, resulting in its degradation by ubiquitin and proteasomes. In contrast, inhibition of GSK 3β activity via Wnt stimulation allows β-catenin to accumulate in the cytoplasm and enter the nucleus [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

Treated dentin matrix induces odontogenic differentiation of dental pulp stem cells via regulation of Wnt/β-catenin signaling

Liu

Sun

Yuan

et al. 2022

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“…Abnormalities in the Wnt signaling pathway are associated with a variety of tumor types, including colon cancer[ 30 , 31 ]. The Wnt pathway is classified into canonical and noncanonical pathways; the former of which is β-catenin dependent[ 32 ].…”

Section: Discussionmentioning

confidence: 99%

RBBP4 promotes colon cancer malignant progression via regulating Wnt/β-catenin pathway

Zhu

2020

WJG

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BACKGROUND Our previous study demonstrated that RBBP4 was upregulated in colon cancer and correlated with poor prognosis of colon cancer and hepatic metastasis. However, the potential biological function of RBBP4 in colon cancer is still unknown. AIM To investigate the biological role and the potential mechanisms of RBBP4 in colon cancer progression. METHODS Real-time polymerase chain reaction and western blot analysis were used to detect the expression of RBBP4 in colon cancer cell lines. The cell proliferation and viability of SW620 and HCT116 cells with RBBP4 knockdown was detected by Cell Counting Kit-8 and 5-ethynyl-2’-deoxyuridine staining. The transwell assay was used to detect the invasion and migration capabilities of colon cancer cells with RBBP4 knockdown. Flow cytometry apoptosis assay was used to detect the apoptosis of colon cancer cells. Western blotting analysis was used to detect the expression of epithelial-mesenchymal transition and apoptosis related markers in colon cancer. The nuclear translocation of β-catenin was examined by Western blotting analysis in colon cancer cells with RBBP4 knockdown. The TOPFlash luciferase assay was used to detect the effect of RBBP4 on Wnt/β-catenin activation. The rescue experiments were performed in colon cancer cells treated with Wnt/β-catenin activator LiCl and RBBP4 knockdown. RESULTS We found that RBBP4 was highly expressed in colon cancer cell lines. The 5-ethynyl-2’-deoxyuridine assay showed that knockdown of RBBP4 significantly inhibited cell proliferation. RBBP4 inhibition reduced cell invasion and migration via regulating proteins related to epithelial-mesenchymal transition. Knockdown of RBBP4 significantly inhibited survivin-mediated apoptosis. Mechanistically, the TOPFlash assay showed that RBBP4 knockdown increased activity of the Wnt/β-catenin pathway. Meanwhile, RBBP4 knockdown suppressed nuclear translocation of β-catenin. With Wnt/β-catenin activator, rescue experiments suggested that the role of RBBP4 in colon cancer progression was dependent on Wnt/β-catenin pathway. CONCLUSION RBBP4 promotes colon cancer development via increasing activity of the Wnt/β-catenin pathway. RBBP4 may serve as a novel therapeutic target in colon cancer.

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“…WLS is an important regulator of Wnt signaling [ 90 , 91 ], a well-known pathway of which dysregulation has been linked to tumorigenesis and progression of various types of malignant tumors [ 7 , 8 ]. Recent studies on oral cancer indicate both the canonical and non-canonical Wnt pathways as targets of multiple miRNAs, including miR-329, miR-410 and miR-21 [ 21 , 104 ].…”

Section: Discussionmentioning

confidence: 99%

“…In addition to its endogenous activity during development, abnormal regulation of Wnt signaling has been implicated in a number of human diseases, including cancer. For instance, enhanced signaling of the Wnt/β-catenin pathway is one of the most common cellular hallmarks detected in the majority of cancers [ 7 , 8 ]. Initiation of canonical Wnt signaling triggers transcription of several effector genes important for tumorigenesis and cancer progression, including c-MYC and cyclin D1 [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-31 Regulates Expression of Wntless in Both Drosophila melanogaster and Human Oral Cancer Cells

Jung

Lee

Kim

et al. 2020

IJMS

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Recent comparative studies have indicated distinct expression profiles of short, non-coding microRNAs (miRNAs) in various types of cancer, including oral squamous cell carcinoma (OSCC). In this study, we employed a hybrid approach using Drosophila melanogaster as well as OSCC cell lines to validate putative targets of oral cancer-related miRNAs both in vivo and in vitro. Following overexpression of Drosophila miR-31, we found a significant decrease in the size of the imaginal wing discs and downregulation of a subset of putative targets, including wntless (wls), an important regulator of the Wnt signaling pathway. Parallel experiments performed in OSCC cells have also confirmed a similar miR-31-dependent regulation of human WLS that was not initially predicted as targets of human miR-31. Furthermore, we found subsequent downregulation of cyclin D1 and c-MYC, two of the main transcriptional targets of Wnt signaling, suggesting a potential role of miR-31 in regulating the cell cycle and proliferation of OSCC cells. Taken together, our Drosophila-based in vivo system in conjunction with the human in vitro platform will thus provide a novel insight into a mammal-to-Drosophila-to-mammal approach to validate putative targets of human miRNA and to better understand the miRNA-target relationships that play an important role in the pathophysiology of oral cancer.

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Wnt Signaling: Paths for Cancer Progression

Cited by 16 publications

References 109 publications

Treated dentin matrix induces odontogenic differentiation of dental pulp stem cells via regulation of Wnt/β-catenin signaling

Treated dentin matrix induces odontogenic differentiation of dental pulp stem cells via regulation of Wnt/β-catenin signaling

RBBP4 promotes colon cancer malignant progression via regulating Wnt/β-catenin pathway

MicroRNA-31 Regulates Expression of Wntless in Both Drosophila melanogaster and Human Oral Cancer Cells

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